Preparing your results

Our searching services are busy right now. Your search will reload in five seconds.

X
Forgot Password

If you have forgotten your password you can enter your email here and get a temporary password sent to your email.

SOD1 integrates signals from oxygen and glucose to repress respiration.

Cell | Jan 17, 2013

http://www.ncbi.nlm.nih.gov/pubmed/23332757

Cu/Zn superoxide dismutase (SOD1) is an abundant enzyme that has been best studied as a regulator of antioxidant defense. Using the yeast Saccharomyces cerevisiae, we report that SOD1 transmits signals from oxygen and glucose to repress respiration. The mechanism involves SOD1-mediated stabilization of two casein kinase 1-gamma (CK1γ) homologs, Yck1p and Yck2p, required for respiratory repression. SOD1 binds a C-terminal degron we identified in Yck1p/Yck2p and promotes kinase stability by catalyzing superoxide conversion to peroxide. The effects of SOD1 on CK1γ stability are also observed with mammalian SOD1 and CK1γ and in a human cell line. Therefore, in a single circuit, oxygen, glucose, and reactive oxygen can repress respiration through SOD1/CK1γ signaling. Our data therefore may provide mechanistic insight into how rapidly proliferating cells and many cancers accomplish glucose-mediated repression of respiration in favor of aerobic glycolysis.

Pubmed ID: 23332757 RIS Download

Mesh terms: Amino Acid Sequence | Casein Kinase I | Cell Line | Glucose | Glycolysis | Humans | Hydrogen Peroxide | Molecular Sequence Data | Oxygen | Saccharomyces cerevisiae | Saccharomyces cerevisiae Proteins | Signal Transduction | Superoxide Dismutase | Superoxides

Research resources used in this publication

None found

Research tools detected in this publication

None found

Data used in this publication

None found

Associated grants

  • Agency: NIGMS NIH HHS, Id: F32 GM 093550
  • Agency: NIGMS NIH HHS, Id: F32 GM093550
  • Agency: NIGMS NIH HHS, Id: GM50016
  • Agency: NIEHS NIH HHS, Id: P30 ES003819
  • Agency: NIGMS NIH HHS, Id: R37 GM050016

Publication data is provided by the National Library of Medicine ® and PubMed ®. Data is retrieved from PubMed ® on a weekly schedule. For terms and conditions see the National Library of Medicine Terms and Conditions.